ArticleOncogene2006
E2F1 induces MRN foci formation and a cell cycle checkpoint response in human fibroblasts.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- DNA damage response(DDR): a link between cellular senescence and human cytomegalovirus.Virology journal · 2023Review
- CDK2 regulates collapsed replication fork repair in CCNE1-amplified ovarian cancer cells via homologous recombination.NAR cancer · 2023Article
- Acquired genetic changes in human pluripotent stem cells: origins and consequences.Nature reviews. Molecular cell biology · 2020Review
- SAMHD1 Functions and Human Diseases.Viruses · 2020Review
- Programmed expression of pro-apoptotic BMCC1 during apoptosis, triggered by DNA damage in neuroblastoma cells.BMC cancer · 2019Article
- Loss of the tumor suppressor BIN1 enables ATM Ser/Thr kinase activation by the nuclear protein E2F1 and renders cancer cells resistant to cisplatin.The Journal of biological chemistry · 2019Article
- Review
- The Rb binding domain of HPV31 E7 is required to maintain high levels of DNA repair factors in infected cells.Virology · 2017Article
- Mechanisms of hepatocarcinogenesis in chronic hepatitis C.Hepatic oncology · 2014Review
- Tug of war between survival and death: exploring ATM function in cancer.International journal of molecular sciences · 2014Review
- ATM mediates pRB function to control DNMT1 protein stability and DNA methylation.Molecular and cellular biology · 2013Article
- Sp1 facilitates DNA double-strand break repair through a nontranscriptional mechanism.Molecular and cellular biology · 2012Article
- RB: mitotic implications of a tumour suppressor.Nature reviews. Cancer · 2012Review
- Bypass of cell cycle arrest induced by transient DNMT1 post-transcriptional silencing triggers aneuploidy in human cells.Cell division · 2012Article
- Understanding pRb: toward the necessary development of targeted treatments for retinoblastoma.The Journal of clinical investigation · 2012Review
- Network calisthenics: control of E2F dynamics in cell cycle entry.Cell cycle (Georgetown, Tex.) · 2011Review
- pRB, a tumor suppressor with a stabilizing presence.Trends in cell biology · 2011Review
- Cellular aging and cancer.Critical reviews in oncology/hematology · 2011Review
- Dynamics of the transcriptome response of cultured human embryonic stem cells to ionizing radiation exposure.Mutation research · 2011Article
- An E2F1-mediated DNA damage response contributes to the replication of human cytomegalovirus.PLoS pathogens · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Deregulation of the Rb/E2F pathway in human fibroblasts results in an E2F1-mediated apoptosis dependent on Atm, Nbs1, Chk2 and p53. Here, we show that E2F1 expression results in MRN foci formation, which is independent of the Nbs1 interacting region and the DNA-binding domain of E2F1. E2F1-induced MRN foci are similar to irradiation-induced foci (IRIF) that result from double-strand DNA breaks because they correlate with 53BP1 and gammaH2AX foci, do not form in NBS cells, do form in AT cells and do not correlate with cell cycle entry. In fact, we find that in human fibroblasts deregulated E2F1 causes a G1 arrest, blocking serum-induced cell cycle progression, in part through an Nbs1/53BP1/p53/p21(WAF1/CIP1) checkpoint pathway. This checkpoint protects against apoptosis because depletion of 53BP1 or p21(WAF1/CIP1) increases both the rate and extent of apoptosis. Nbs1 and p53 contribute to both checkpoint and apoptosis pathways. These results suggest that E2F1-induced foci generate a cell cycle checkpoint that, with sustained E2F1 activity, eventually yields to apoptosis. Uncontrolled proliferation due to Rb/E2F deregulation as well as inactivation of both checkpoint and apoptosis programs would then be required for transformation of normal cells to tumor cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.